Alterations of the hormone-receptors on or within cells will modify the response of target tissues to various hormones thus serving to control cellular growth or function. We have shown that PRL up-regulates its own receptors by modifying target membrane fluidity and that this may occur through modification of prostaglandin synthesis. Extended to the DMBA rat mammary tumor, the regressing tumor membranes are more viscous and bind less PRL than those of the growing tumor. An assay for PG receptor has been developed, which has demonstrated both that these regressing tumors have increased capacity to bind PG and that copper increases this binding capacity 8-fold. Copper may, thus augment the effect of prostaglandins in vivo and play a role in tumor growth. Patients afflicted with adrenoleukodystrophy or adrenomyeloneuropathy have an inborn propensity to accumulate long chain saturated fatty acids in their cellular membranes. We have demonstrated that this occurs wih erythrocytes and thus alters the fluidity of these membranes. Such changes in membrane may reflect similar changes within the adrenal and gonads and may account for the states of adrenal and gonadal failure observed in these patients. Thus, our studies show quite clearly that membrane-associated receptors are modulated by alteration of membrane fluidity. Metabolism of arachidonic acid by six human tumorss is directed toward the lipoxygenase pathway in preference to that of the prostaglandins. The synthesis of prostaglandins by these tumors appears to be determined by relative deficiences in PGF2Alpha isomerase and probable deficiency in phospholipase A2 and/or cycloxygenase activity. Each tumor type metabolizes arachidonic acid in an unique fashion suggesting that various modes of therapeutic may be employed through the use of agents that inhibit specific enzymes within these pathways.